Kainate induces mobilization of synaptic vesicles at the growth cone through the activation of protein kinase A.

Giuliana Gelsomino, Elisabetta Menna, Flavia Antonucci, Simona Rodighiero, Loredana Riganti, Christophe Mulle, Fabio Benfenati, Flavia Valtorta, Claudia Verderio, Michela Matteoli
Cerebral Cortex. 2012-03-07; 23(3): 531-541
DOI: 10.1093/cercor/bhs026

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1. Cereb Cortex. 2013 Mar;23(3):531-41. doi: 10.1093/cercor/bhs026. Epub 2012 Mar 7.

Kainate induces mobilization of synaptic vesicles at the growth cone through the
activation of protein kinase A.

Gelsomino G(1), Menna E, Antonucci F, Rodighiero S, Riganti L, Mulle C, Benfenati
F, Valtorta F, Verderio C, Matteoli M.

Author information:
(1)Department of Medical Pharmacology and Consiglio Nazionale delle Ricerche
(CNR) Institute of Neuroscience, University of Milano, 20129 Milano, Italy.

Activation of protein kinase A (PKA) pathway at presynaptic terminals plays a
crucial role in the supply of synaptic vesicles (SVs) from the reserve pool,
affecting the steady-state level of activity and the reconstitution of the
readily releasable pool after intense stimulation. However, the identity of the
stimuli activating this pathway is undefined. Using fluorescence resonance energy
transfer and molecular genetic, we show that kainate, through the activation of
presynaptic kainate receptors, induces PKA activation and enhances synapsin I
phosphorylation at PKA-specific residues. This leads to a dispersion of synapsin
I immunoreactivity, which is accompanied by a PKA-dependent increase in the rate
of SV recycling at the growth cone and by an enhanced miniature excitatory
postsynaptic currents frequency in mature networks. Selective activation of this
pathway is induced by the native neurotransmitter glutamate, when applied in the
high nanomolar range. These data identify glutamate, specifically acting on KARs,
as one of the stimuli able to induce phosphorylation of synapsin at PKA sites,
both at the axonal growth cone and at the mature synapse, thus increasing SV
availability and contributing to plasticity phenomena.

DOI: 10.1093/cercor/bhs026
PMID: 22402347 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus